Europace Advance Access originally published online on July 16, 2007
Europace 2007 9(8):578-584; doi:10.1093/europace/eum132
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BASIC SCIENCE
The effect of streptomycin on stretch-induced electrophysiological changes of isolated acute myocardial infarcted hearts in rats
Department of Cardiology, the First Hospital of Harbin Medical University, Harbin, Heilongjiang Province 150001, China
Manuscript submitted 8 February 2007. Accepted after revision 8 June 2007.
* Corresponding author. Tel: +86 451 53643849-5473. E-mail address: junxiancao{at}gmail.com
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Abstract |
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Aims To explore whether the stretch of ischaemic myocardium could modulate the electrophysiological characteristics, especially repolarization via mechanoelectric feedback (MEF), as well as the effect of streptomycin (SM) on these changes.
Methods Thirty-six wistar rats were randomly divided into four groups: control group (n = 9), SM group (n = 9), myocardial infarction (MI) group (n = 9), and MI + SM group (n = 9). After perfused on Langendorff, the isolated hearts were stretched for 5s by a ballon inflation of 0.2mL. After being stretched, the effect of the stretch was observed for 30s, including the 20, 20–70, 70, and 90% monophasic action potential duration (MAPD), i.e. MAPD20, MAPD20–70, MAPD70, and MAPD90, respectively, premature ventricular beats (PVB), and ventricular tachycardia (VT).
Results The stretch caused a decrease in MAPD20–70 (both P <0.01) and an increase in MAPD90 (both P <0.01) in both control and MI groups. Moreover, the MAPD90 in the MI group had increased more significantly than that in the control group (P <0.05). A concentration of 200 µmol/L of SM had no influence on both MAPD20–70 and MAPD90 of basic state (P > 0.05, except MAPD20–70 between the control and SM groups, P < 0.01), whereas it had reduced the length of MAPD90 (P < 0.05) and inhibited the decrease in MAPD20–70 induced by the inflation. There was a decrease in the tendency of MAPD70 after the stretch (P = NS) and SM had reversed the tendency, whereas MAPD20 had no obvious changes after inflation. The incidence rate of PVB and VT in the MI group was higher than that in the control group after inflation (P < 0.01). The 200 µmol/L SM reduced the incidence rate of PVB, and obviously inhibited the occurrence of VT (P < 0.01).
Conclusions Stretch could alter the electrophysiological activities of myocardium via MEF, which could enhance in acute myocardial infarction and facilitate the generation and maintenance of malignant arrhythmias. SM could significantly inhibit the occurrence of arrhythmias, which may correlate with the effect on blocking stretch-activated ion channels.
Key Words: Streptomycin, Arrhythmia, Monophasic action potential, Infarction, Ion channels, Stretch/mechanoelectric coupling
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Introduction |
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Myocardial stretch can initiate the changes of myocardial electrophysiological properties, which is called mechanoelectric feedback (MEF).1
–2 The changes include the shortening of both the action potential duration (APD) and the effective refractory period, the production of after-depolarization and triggered activity.3 The decrease in the early repolarization and the increase in the late repolarization4 are also included. However, the mechanism was not so clear. Normally, the well-known explanation is transmembrane ion fluxes through stretch-activated ion channels (SACs). SACs have been found in both atrium and ventricle of various species, such as canine, rabbit, pig, rat, frog, human, and guinea pig.2,3,5–9 The characteristics of SACs and the important role SACs play in stretch-induced arrhythmias (SIAs) have been described in detail by Sackin.10 Using the blockers of SACs, streptomycin (SM), many studies have demonstrated that SACs were involved in the changes of stretch-induced myocardial electrophysiological properties in normal cardiac tissues.11,12
On the basis of the data from clinical observation, there is a high incidence of cardiac arrhythmias and sudden death in patients with diseased myocardium, especially left ventricular hypertrophy,13 heart failure,14 myocardial ischaemia,15 and hearts transplanted by autologous skeletal muscle cell.16 Furthermore, above all that had been mentioned existed the ventricular asynchrony that produced the stretch of myocardium and subsequent MEF during cardiac cycle. Moreover, Parker et al.17 and Pye and Cobbe18 have respectively ensured the existence of MEF in hypertrophic and failed myocardium. Kiseleva et al.3 have further studied the role of MEF and SACs in complex arrhythmia with slices from chronic infarcted myocardium. They found that MEF could be enhanced in post-infarcted myocardium comparing with normal cardiac muscle. However, it could bring fatal arrhythmia like ventricular fibrillation (VF),21 if regional inhomogeneities in contractility and mechanical restitution, serving as foci for SIAs, have already existed early in acute myocardial ischaemia.19,20 From the above, it is hypothesized that in acute myocardial ischaemia, rapid left ventricular distention could induce regional inhomogeneities, which might be the foundation of MEF and SACs; at the same time, MEF could contribute to the electrophysiological changes.
The purpose of this study was to explore the changes of monophasic action potential (MAP) induced by stretch during acute myocardial infarction (AMI), especially in repolarization, as well as the effect of SM on SIAs and stretch-induced MAP changes with isolated hearts in rats.
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Langendorff perfusion
A total of 36 Wistar rats (without limitation on the gender), weighing between 190 and 260g, were anaesthetized with sodium pentobarbital (40–50mg/kg) mixed with heparin (1000 U/kg) via ip injection. The heart was harvested and immediately placed in 4°C Tyrode's solution; then perfused using Langendorff apparatus via the aorta; the time taken from heart excision to establishment of perfusion was <2 min. The solution was heated to 37°C by a temperature control system [HSS-1(B), ChengDu, China] and oxygenized with 95% O2–5% CO2. The experiments were conducted strictly according to the international guidelines on animal experiments.
A fluid-filled latex balloon, connected with a pressure transducer (GaoBeiDian, China), was inserted into the left ventricle (LV). The distance between the balloon and the transducer was minimized to prevent system dampening. The preliminary volume of the balloon was 0.05mL, maintaining the end diastolic pressure.
Experimental solutions
The Tyrode's solutions consisted of (mmol/L): NaCl 118.5, NaHCO3 25, KCl 4.7, MgSO4·7H2O 1.2, KH2PO4 1.2, CaCl2·2H2O 1.4, Glucose 11.0, and pH was adjusted with NaOH to 7.4. SM was dissolved in Tyrode's solution to give a concentration of 200 µmol/L.
Stimulation and recordings
Suction electrodes consisted of metal filaments and a silica gel tube. The inner and outer diameters of the silica gel tube were, respectively, 1 and 1.5 mm. The metal filaments were achieved through welding platinum with the silver filaments. The end of the sliver piece, passing through the wall of the tube, was connected with an input link to detect the electrical signal. A vacuum was applied via the thin silica gel tube. Suction electrodes on the anterior wall of the LV were used to detect the LV MAP. The heart was paced at 3 Hz via a pair of bipolar pacing electrodes inserted into the right ventricle (RV). The preparation was paced using a square wave of 2 ms duration with an amplitude twice the stimulation threshold.
These electrical signals were passed to a DC amplifier (Med4101, Nanjing Medease Science and Technology Co. LTD, China), digitized at 3 kHz with a recording bandwidth of DC 500 Hz using a 12-bit analogue-to-digital (A/D) converter (NSA4, Nanjing Medease Science and Technology Co. LTD, China) and stored on a computer for subsequent data analysis. The signals were monitored in real time during the experiment.
Experimental protocols
The heart was perfused in Tyrode's solution for 
15 min to allow stabilization. Each sequence of the electromechanical stimulation was initiated by a train of beats at the frequency of 3 Hz. Then, a transient stretch (5 s) begun with diastolic phase was delivered by an increase in the LV balloon volume (
V = 0.2mL), followed by a return to the initial volume. The MAPs, LV pressure, maximum rate of change of pressure (dp/dtmax), and arrhythmia were monitored for 30 s after returning to its initial volume.
The hearts were divided into four groups: (1) control group (n = 9), experiments were conducted after stabilization for 15 min; (2) SM group (n = 9), experiments were conducted after SM perfusion for 15 min; (3) MI group (n = 9), experiments were conducted by ligation of the left anterior descending branch (LAD) for 30 min; (4) MI + SM group (n = 9), experiments were conducted after 15 min SM perfusion followed by ligation of LAD for 30 min.
Data analysis
Monophasic action potential duration (MAPD) (in ms) at 20, 70, and 90% repolarization (MAPD20, MAPD70, and MAPD90) of LV was measured semiautomatically, meaning that the period for analysis was manually selected by two cursors and MAPD20, MAPD70, as well as MAPD90 was measured automatically using the MatLab software (MathWorks Company, Natick, USA), MAPD20–70 = MAPD70–MAPD20. We analysed one MAP every nine beats and calculated the mean. SIAs were defined as MAPs with the guidelines of the Lambeth convention.22 The data analysis was conducted by an independent university-based statistician with SPSS13.0 (Statistical Package for the Social Sciences 13.0, SPSS company, USA). Quantitative data were reported as mean ± SD and compared with ANOVA. Qualitative data were compared with a 
2 test. Differences with a value of P <0.05 were considered statistically significant.
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Results |
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The effect of stretch on monophasic action potential
The value of MAPD20–70 decreased after stretch in the control group (from 22.37 ± 4.76 to 16.04 ± 3.76 ms, P < 0.01) and MI group (from 22.09 ± 3.33 to 16.94 ± 3.85 ms, P < 0.01), whereas the value of MAPD90 increased under the same conditions (from 37.62 ± 2.92 to 52.46 ± 3.87 ms in the control group, P < 0.01; from 45.76 ± 3.96 to 58.09 ± 4.27 ms in the MI group, P < 0.01). There was no significant difference in the MAPD20–70 value between the control and MI groups in basal condition (22.37 ± 4.76 vs. 22.09 ± 3.33 ms, P > 0.05), likewise after inflation (16.04 ± 3.76 vs. 16.94 ± 3.85 ms, P>0.05) (Table 1; Figure1).
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There was no obvious difference in MAPD20 and MAPD70 between the control and MI groups, respectively, in the basal condition (for MAPD20, 7.23 ± 3.13 vs. 9.54 ± 3.03 ms; for MAPD70, 29.56 ± 6.30 vs. 31.63 ± 3.12 ms, both P > 0.05), as was so after inflation (for MAPD20, 8.63 ± 2.21 vs. 11.22 ± 2.78 ms; for MAPD70, 25.88 ± 4.75 vs. 28.17 ± 4.52 ms, both P > 0.05). And, in normal and infarcted rat hearts, no significant change in MAPD20 and MAPD70 appeared, either (in control group: MAPD20, from 7.23 ± 3.13 to 8.63 ± 2.21 ms; MAPD70, from 29.56 ± 6.30 to 25.88 ± 4.75 ms. In MI group: MAPD20, from 9.54 ± 3.03 to 11.22 ± 2.78 ms; MAPD70, from 31.63 ± 3.12 to 28.17 ± 4.52 ms, both P>0.05) (Table 1).
However, MAPD90 showed an obvious change after ligation of LAD for 30 min. After inflation, MAPD90 in the MI group increased much more significantly than that in the control group (58.09 ± 4.27 vs. 52.46 ± 3.87 ms, P <0.05). In basal condition, MAPD90 also increased in the MI group (Table 1; Figure 1).
The effect of streptomycin on monophasic action potential duration changes after inflation
In basal conditions, SM had no influence on MAPD90 and MAPD20–70 both in normal and infarcted rat hearts (except MAPD20–70 between control and SM groups, 22.37 ± 4.76 vs. 15.4 ± 4.74 ms, P <0.01). SM inhibited the decrease in MAPD20–70 caused by inflation; nonetheless, little increase was recorded, however (P>0.05, in the SM group, from 15.4 ± 4.74 to 19.98 ± 7.26 ms, and in the MI + SM group, from 19.66 ± 4.89 to 21.93 ± 6.61 ms). As so in MAPD90, SM had reduced the length of MAPD90 (control vs. SM group, 52.46 ± 3.87 vs. 46.19 ± 2.87 ms; MI vs. MI + SM group, 58.09 ± 4.27 vs. 53.1 ± 3.64 ms, both P <0.05) (Table 1; Figure 1).
Streptomycin reversed the reducing tendency of MAPD70. There also existed a slight increase in MAPD70 from 22.16 ± 5.18 to 28.27 ± 7.27 ms in the SM group and from 30.50 ± 5.96 to 31.8 ± 6.33 ms in the MI + SM group, both P > 0.05. As for MAPD20, it seemed that SM posed no obviously definite effect (from 6.68 ± 0.93 to 8.29 ± 2.93 ms in the SM group; from 10.84 ± 4.65 to 9.87 ± 4.17 ms in the MI + SM group, both P > 0.05) (Table 1).
The effect of streptomycin on stretch-induced arrhythmias
The premature ventricular beats (PVB) were caused by inflation of the balloon. In normal hearts, the number of PVB was 19. After ligation of LAD for 30 min, it significantly increased to 53—nearly three times than that of the control group (P <0.01). SM significantly decreased the occurrence of PVB induced by stretching from 19 to 7 in normal hearts (P <0.05) and from 53 to 25 in infarcted hearts (P <0.01) (Table 2). The figures of MAP were recorded by signal-collected systems (Figure 2).
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Caused by the stretch under the condition of
V = 0.2mL, the number of VT in the control, SM, as well as MI + SM groups was all equal to 0, whereas the number of VT in the MI group increased to 4. There existed significant difference between MI group and control group (P < 0.01); and SM inhibited the appearance of VT (MI + SM group vs. MI group, P < 0.01) (Table 3).
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Discussion |
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The results of the study have demonstrated that in isolated rat hearts (1
) during the early stage of AMI, mechanical stretch of myocardium could decrease MAPD20–70 and increase MAPD90, which is much more easily to be induced than the hearts of normal rats. Simultaneously, unlike MAPD20–70 or MAPD90, MAPD20 and MAPD70 had not changed obviously after stretch. (2) Stretching the acute infarcted myocardium can cause a higher incidence in SIAs, especially in the complex arrhythmias. (3) SIAs and the changes of MAPD which could be suppressed by SM indicated the involvement of SACs in MEF of AMI.
Stretch-induced monophasic action potential duration changes and arrhythmias
The stretch-induced changes of MAPD have been found in cardiac tissues or cells of many species.23–25 The present study showed that the changes of MAPD caused by stretch in AMI were consistent with the tendency appearing in normal myocardium. MAPD20–70 decreased and MAPD90 increased after stretch both in normal and acute infarcted myocardium. These changes of MAPD were in line with the characteristics of SACs as opinions of Hansen et al.26
Kiseleva et al.3 had found that MEF were enhanced in chronic myocardial infarction by use of Gd3+, another kind of SACs blocker. The present study furthermore found that in AMI, the longer MAPD90 and the shorter MAPD20–70 were induced with stretch of the same extent compared with normal myocardium. So did the SIAs. Therefore, the activities of SACs and MEF were inferred to be enhanced in AMI.
It is well known that the dilation of the ischaemic region was independently associated to VF21 and that regional ventricular ischaemia increased the occurrence of arrhythmia with transient stretch.27 Ischaemic myocardium has a lower contraction force than surrounding normal myocardium within minutes of acute myocardial ischaemia,28,29 which may be stretched in the whole ventricular wall motion during cardiac cycle. As we all know, mechanical stimulus could pass to the mechanoelectric transducers via integrin, cytoskeleton, and other structures that were associated with mechanical transduction. The appearance and characteristics of these structures would change with various degrees in ischaemic myocardium,30 which could enhance the activities of SACs.31 The changes of these structures could also facilitate the formation of MEF.
The results of this study showed that MAPD70 decreased after stretch and with a tendency of prolongation by using SM, despite the insignificant difference (P = 0.057), which might be of lesser samples. On the basis of the formulation MAPD70 = MAPD20–70+MAPD20 and the data from this study, it is concluded that the reduction in MAPD70 was mainly caused by the shortened MAPD20–70. It was inferred that the activities of SACs mainly influenced the preferred intermediate stage of repolarization over the early stage. The possible mechanisms might include: (1) there existed stretch-inactivated ion channels,32,33 whose activities in the early stage of repolarization is as same of activities causing by SACs. (2) The variability in SACs may play an important role in the phenomena as we have observed. Several kinds of SACs may exist in one cardiomyocyte.34 The different reversed potentials of SACs and the different duration of SACs in open state could influence the changes of MAPD.34
The effect of streptomycin on monophasic action potential duration and stretch-induced arrhythmias
In single cardiomyocyte11 and multicellular preparations,12,35 SM has proved to be a potent blocker of SACs. The present study has provided the initial evidence that the changes of MAPD in AMI that were induced by stretch could be pharmacologically modulated by an SAC-blocking agent. SM effectively inhibited or reversed the reduction in MAPD20–70 and the increase in MAPD90 both in normal and acute ischaemic myocardium. The reduction in MAPD70 also showed the tendency of prolongation by using SM. Moreover, SM reduced/inhibited PVB and VT caused by inflation. Consequently, SACs might be involved in MEF during AMI.
Of many theories on SIAs, the main explanation is the increase in intracellular Ca2+ ([Ca2+]i) caused by stretch.36 Stretch brings to open SACs which allows extracellular Ca2+ and Na+ to enter the cells, favouring the opening of L-type Ca2+ channel and sarcoplasmic reticulum Ca2+ release. An inward current, Na+–Ca2+ exchange current (NCX), may arise from the entry and release of Ca2+, leading to after-depolarization and triggered activity.37 The anti-arrhythmia effect of SM might lie in a fall of [Ca2+]i with blocking SACs because at this concentration, disallowing SM to affect the L-type Ca2+ current.38
The results of this study revealed that many fatal arrhythmias may be caused by mechanical disorders. If the role of MEF in the production and maintenance of arrhythmias could be sufficiently confirmed, the future therapeutic programme would not be restricted to classical anti-arrhythmic agents. More attention should be paid to rectify these abnormalities of mechanical activities for prevention or termination of malignant arrhythmias.
Limitation
The effect of SM on inhibiting the stretch-induced electrophysiological changes potentially demonstrated the involvement of SACs during stretch. However, SACs may not be the only factor in MEF.39,40 Other mechanosensitive channels and transmural heterogeneity of channels41 may also involved in the observed electrophysiological abnormalities. Moreover, the sensitivity to SM of these channels has not yet been known. And, the MAP in rats is not completely coincide with that of humans. Following this, further study should be performed to confirm the relationship between stretch and arrhythmias.
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Acknowledgements |
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The authors would like to thank Li Shu-xue (Heilongjiang University of Traditional Chinese Medicine,Harbin), Qu Fan (Heilongjiang University of Traditional Chinese Medicine,Harbin), Han Si-ying (Harbin Medical University, Harbin), and Ning Chun-ping (Harbin Medical University, Harbin) for their reviews and suggestions on this paper. We give our especial thanks to Mark Jones (Heilongjiang University, Harbin) for his revision on language. This work was supported by the Innovative Research Foundation for postgraduates by the Government of Heilongjiang Province, China (SCX2005014).
Conflict of interest: none declared.
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Footnotes |
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This study was performed in the central laboratory of angio-cardiopathy institute of the First Hospital of Harbin Medical University, Harbin, China. 
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References |
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